An essay about the rabies virus and its treatments.

The disease rabies is a viral infection caused by the Lyssavirus of the Rhabdoviruses family. Rhabdoviruses are rod-shaped viruses that can be up to 100 nanometers in diameter and 400 nanometers long. These viruses consist of only five different proteins, the G protein, M protein, N protein, L protein, and P protein. The G proteins are transmembrane protein and about 1200 of them form the surface of a single virus. The matrix (M) proteins, line the inner surface of the viral membrane, protecting the nucleocapsid inside. The nucleocapsid is made up of the N, P, and L proteins. The N (nucleoprotein) protein surrounds and protects the genome, the L protein and P protein together make up the RNA polymerase, necessary for viral replication. Viral replication consists of five steps. First, the virus binds to receptors of the host organism. Then, the virus penetrates the nuclear membrane of a host cell, and the nucleocapsid enters the cytoplasm. Once the virus is inside, transcription occurs, creating mRNA molecules for each of the respective proteins. Afterwards, replication occurs, using unzipped RNA molecules as a template for the creation of new RNA molecules. Then, new virus molecules are assembled by translation of the mRNA strands, synthesizing new protein molecules which come together to form a complete virus. After the cycle is complete the nucleocapsid bursts through the cell membrane of the host. The rabies virus is most commonly transmitted through the saliva of infected animals, predominantly through their bites. Rabies is also less commonly spread by contact with an open wound, transplant of infected tissues, and very rarely by inhalation of an aerosolized form of the virus. Many mammals are potential carriers of the virus, including dogs, raccoons, skunks, foxes, and bats. Smaller mammals, such as rats, are rarely carriers of the virus because a bite from an infected animal would likely be fatal. Diagnosis of rabies through examination of obvious symptoms is fundamentally useless because the disease is almost inevitably fatal by that point; as only six cases of survival of symptomatic rabies have been recorded. Fortunately, there are several other methods that can be used for diagnosis of the disease. A skin or brain biopsy can be tested for the antigen using a direct fluorescent antibody test. Alternatively, saliva can be tested for the virus by reverse transcription-polymerase chain reaction, or isolation of the virus. In an infected animal, the virus binds to nerve or muscle cells at the site of inoculation via nicotinic acetylcholine receptors. It is there that the virus can replicate without symptoms occurring, this is known as the incubation period. After transmission, symptoms usually begin to occur after a one to three month incubation period, although the incubation period can be as short as a few days or as long as several years. Once the incubation period ends, the virus moves using retrograde transport through nerve axons along to the central nervous system, and arrives at the central root ganglia and spinal cord. Once the virus reaches that portion of the central nervous system, the virus begins to spread inside the brain of the host animal. Once there, the virus infects many several different cells, including cells of the cerebellum and hippocampus, as well as the pontine nuclei. This early stage of viral infection of the brain is known as the prodromal phase. Infection of the brain causes neural degeneration as well as encephalitis, swelling of the brain tissue. These occurrences within the brain characterize the neurological phase of rabies, and nearly always lead to coma and death. During the neurological phase, the virus spreads from the central nervous system to the skin, eyes, and internal viscera through neurons. Ironically, rabies causes very little in terms of cytopathic damage outside the brain. The primary factors which affect the onset of symptomatic rabies are the number of virus particles in the infection, as well as the nearness of the infection to the brain.   However, the natural human immune response does little to prevent the onset of rabies, due to the fact that development of immune response occurs very slowly, and does not work effectively until after the rabies virus reaches the brain, which generally is too late for survival.  Symptoms begin to occur once the rabies virus reaches the brain of the host animal and begins to rapidly multiply there. In animals, signs that an animal may be affected by the rabies virus include drooling, foaming at the mouth, and paralysis. Animals affected by rabies may also behave unusually. A pet that is afflicted by rabies may act shy toward humans; alternatively, some wild animals lose their fear of humans. Also, some nocturnal animals such as skunks and foxes may come out during the day if rabid.  Early symptoms of the virus in humans are reminiscent of the flu, and include fever, headaches, fatigue, and discomfort or numbness at the site of the bite. As the disease progresses, neurological symptoms begin to occur, including insomnia, anxiety, confusion, and hallucinations, as well as non-neurological symptoms such as difficulty swallowing and hydrophobia. Hydrophobia, the fear of water, seen in rabies patients is a result of pain associated with drinking, due to the swelling of the spinal cord near the throat. In some cases, the only neurological symptom that occurs is paralysis. This paralysis can lead to death through failure of the respiratory system. At the end of the neurological phase the patient becomes comatose and then dies as a result of respiratory failure. However, this tragic outcome can be avoided if proper preventative measures are taken before the onset of symptomatic rabies. Initially, the wound that may be the site of rabies transmission should be thoroughly washed with soap and water. Afterwards it should be treated with ethyl alcohol or an antiseptic such as sodium benzyl ammonium chloride. When treatment of the wound is complete, the State Health authorities have the right to determine whether or not prophylaxis, the vaccine for rabies, should be given to the patient as treatment. One way they determine whether or not this treatment is necessary is by capturing the potentially afflicted animal and examining their brain for the rabies antigen through by fluorescent antibody. However, if the potentially afflicted animal is a domesticated animal it may be kept under close watch for overt symptoms, to prevent killing the animal. If the State Health authorities decide that prophylaxis should be administered, then the vaccine will be administered as a series of shots over a four week long period. Alongside prophylaxis, the human rabies immunoglobin is injected into the patient, with as much as half of the HRIG being injected at the site of the wound. The rest is administered as an intramuscular injection. When prophylaxis and HRIG are administered together, a separate syringe and site of injection are used to ensure that the HRIG does not neutralize the effect of the prophylaxis. If a person exposed to the rabies virus has already been vaccinated with pre-exposure prophylaxis, they will still receive post-exposure prophylaxis, but HRIG will not be administered. Worldwide, approximately 55,000 people die of rabies every year, from a variety of sources through which the disease is transmitted. In North America the most prominent caries are skunks, foxes, raccoons, and especially bats. In South America the disease is most commonly spread by rabid dogs or vampire bats. Throughout Europe rabies is spread predominantly by badgers and foxes. In India, Latin America, and Africa, which account for most of the human deaths caused from rabies each year, rabid dogs are the most frequent carriers of the disease. Thankfully, death from the rabies virus is easily preventable if proper preventative measures are taken. Approximately 40,000 people are treated with the vaccine each year after being exposed to the rabies virus, and there is no documented case of any person developing symptomatic rabies are being treated with post-exposure prophylaxis.

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